Phys Winter #1.txt

11

• Detect
• Integrate
• restore

• Sensor - recognizes signal
• Integrate - interprets signal/instructs
• Effector - communicates

It increases the signal (e.g. oxytocin and increasing contractions)

• Plasma
• Interstitial fluid

• Na⁺= outside of cell (ECF)
• K⁺= inside of cell (ICF)
• Cl^-= outside of cell (ECF)
• Proteins = inside of cell (ICF)

• Water moves from area of low solute concentration to high solute concentration.
• Works only in areas of impermeable solutes.

• Water/solute conc. equal
• No more net movement
• No volume change

• Non-permeable solutes
• Amount of pressure that finally stops diffusion of water

300 mOsm/L

• #osmoles/Liter
• osmoles = # of particles that will dissociate in solution

the effect a solution has on the volume of the cell (hypoosmolar = swell, hyperosmolar = shrink, isoosmolar = steady state)

K⁺ and Cl^-

-Na⁺/H⁺ to bring Sodium in (H⁺ leaving causes the cell to become basic)

-Cl^-/HCO₃^- exchanger (no bicarb needed to cause cell to be basic, so it leaves)

Active Transport requires ATP-energy

Digitalis a.k.a. ouabain (cardiac glycosides)

• 3 Sodium out
• 2 Potassium in

Na⁺/glucose (utilizes the ATP from the Na⁺/K⁺ ATP-ase for its energy gradient to bring glucose against its concentration gradient into the cell)

• 60 L total
• 40 L ICF
• 20 L ECF (3/4 interstitial, 1/4 Plasma)

TBW = .7LBM + .1 AT

The more fat the less water

2Na⁺ + Glucose/18 + BUN/2.8

• Inside = negative
• Outside = positive

Potassium due to more channels

E_k= -90 mV

E_Na⁺= +65mV

E_cl^-= -90mV

E_Ca²⁺= +120mV

E_ion= (60/z) log (ion_out/ion_in)

***used to calculate equilibrium potential

More on K

Hyperpolarize because RMP becomes more negative as well as the equilibrium potential becoming more negative

• E_m= (g_kE_k + g_NaE_Na)/(g_k+g_Na)
• ***shows resting membrane potential

• 1) ligand-gated
• 2) mechanosensitive

Voltage-gated

Bi-directional

Gated change depending on magnitude of stimulus while action are all-or-nothing

It diminishes as it spreads from the center of activation

Unidirectional and it does not dissipate throughout the neuron

Larger diameter (myelin will increase it as well)

Highest concentration of voltage gated channels for action potentials. Must reach threshhold around -60 to -65 before propogating.

-70 mV

• Tetrodotoxin
• Lidocain

Na⁺/K⁺ ATP-ase

• Contiguous: no myelination so potential continues along every fiber
• Saltatory: Jumping from myelin over nodes of Ranvier (faster)

Multiple sclerosis

• The calcium binds to the phospholipids and makes the threshhold potential more positive, therefore, requiring a stronger stimulus to reach threshhold
• muscle weakness

• More easily excitable b/c cells are more negative
• muscle twitching

• Phosphate binds to Calcium and causes a more easily excitable neuron
• hypoparathyroidism

• More free calcium b/c less bound to phosphate = less excitable neurons
• hyperparathyroidism

More hydrogen which leads to more free calcium b/c of competition with binding to negative proteins = less excitable = muscle weakness

Less hydrogen to compete for binding to proteins with calcium = less free calcium = more excitable = muscle twitching

Connexons

Electrical (continuous)

Electrical

H⁺ channels

Ca²⁺ channels

• 1) degradation by AchEsterase
• 2) Reuptake by presynaptic cleft
• 3) diffusion

Graded

Synaptotagmin

Disease that inactivates presynaptic Ca²⁺ channels so no binding of synaptic vesicles or clear vesicles can occur

Neuropeptide (not neurotransmitter)

• Ionotropic: ion channels on postsynaptic cleft
• Metabotropic: G-protein channels

• Block dopamine reuptake
• Block Sodium channels

• Sarcolemma: voltage-gated
• Motor end plate: chemically-gated

Two

Hydrogen pump so the H/Ach pump can function with a gradient

Competitive antagonist against Acb

mimic Ach so muscle is depolarized too much and eventually paralyzed

• Botulism taken up by pre-synaptic cleft
• blocks snare proteins so vesicle does not bind
• no depolarization = muscle weakness

• no Ach degredation
• muscle twitching, followed by flaccid muscles

• antibodies against Ach receptors
• to cure, treat with Achesterase inhibitors so more Ach can compete with the blocking antibodies

Reversible AchEsterase inhibitor (used for MG and after surgeries to recover from muscle relaxants)

• DHP: t-tubule
• RYR: Sarcoplasmic Reticulum

DHP mechanically opens RYR

inhibit binding of myosin to thin actin filaments

• ***Calcium sensor
• TnT: ties together Troponin and Tropomyosin
• Tnl: bound to actin and inhibits ATPase activity
• TnC: senses and binds Calcium

• Titin: ties thick myosin filaments to z-band
• Nebulin: controls length of thin actin filaments

bind actin filaments to sarcolemma cytoskeleton

Muscular Dystrophy = muscle weakness b/c no link for contraction to occur

• RYR
• function: sequester calcium and store it for release, reduces free calcium so excitation can occur

• Utilizing various different motor units to activate movement
• Is good for modulating and maintaining muscle strength

• I : slow, aerobic, endurance
• II : fast, anaerobic, sprint

• Neuronal
• Muscle hypertrophy
• muscle fiber change

Just size, the number of fibers never changes

Early training

If absent, muscle hypertrophy still continues but the tendons are very weak and brittle

loss of skeletal muscle mass and strength due to aging

Type IIx

• motility
• pressure
• flow

• Single-unit
• multi-unit

Varicosities

Single-unit

• Myogenic = single unit = self-excitable with no required neuronal signalling
• Neurogenic = multi-unit = fine control, requires neuronal signalling

Single-unit

• 1) Epinephrine 80%
• 2) Norepinephrine 20%
• 3) Dopamine
• ***all from adrenal medulla
• ***parasym does not release hormones

Sweat Glands: Cholinergic instead of adrenergic

• 1) salivary glands: s = thick,p = watery
• 2) lacrimal: both produce tears
• 3) Sexual: p = erection, s = ejaculation

• 1) Voltage-gated: ECF
• 2) Ligand-gated: ECF
• 3) IP3: SR

• 1) SR Ca-ATPase
• 2) Sarcolemma Na/Ca Exchanger
• 3) Sarcolemma Ca-ATPase